RESUMO
Testosterone, after conversion to estrogen, masculinizes the developing preoptic area (POA) of rats, via binding to intracellular estrogen receptors located within the POA. Our previous studies have shown what seems to be a paradox, in that the levels of estrogen receptor mRNA are lower in males than in females. In the present study, we examined the effects of hormone manipulations on estrogen receptor (ER) mRNA levels in the preoptic area of neonatal male and female rats to test the hypothesis that gonadal steroid hormones regulate ER mRNA during the perinatal period. The relative amount of steady state ER mRNA was assessed in the preoptic area of postnatal day 4 animals using in situ hybridization and film autoradiography. Hybridization density was approximately 2-fold higher in females compared with hybridization density in males. Depletion of testosterone by bilateral removal of the testes on the day of birth increased the level of ER mRNA in males to that observed in females. Treatment of females with the synthetic estrogen, diethylstilbestrol (1 microgram per day, in pellet form), reduced ER mRNA levels to a level comparable to that in intact males. The non-aromatizable androgen, dihydrotestosterone (50 micrograms per day, in pellet form), had no effect on ER mRNA in females. These results suggest that estrogen, derived from the local aromatization of circulating testosterone, down-regulates ER mRNA in the neonatal male preoptic area. Down-regulation of ER mRNA may be an important estrogen-regulated event in the process of sexual differentiation of the preoptic area.
